Hypercatabolism of complement in Crohn's disease--assessment of circulating C3c.
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Summary
Substantially elevated plasma C3c in Crohn's disease suggests hypercatabolism of C3, that is, involvement of complement reactions and further studies are needed to reveal the site of cascade activation and to define the role of complement for the pathogenesis of the disease.
- Type
- article
- Published
- 2009-04-24
- Cited by
- 21
- References
- 19
- OpenAlex
- https://openalex.org/W2032508280
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:44377392
Keywords
Ulcerative colitis, Medicine, Complement (music), Disease, Crohn's disease
References
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- C3 Polymorphism and circulating immune complexes in patients with multiple sclerosis
- A simple index of Crohn's-disease activity.
- A single step immunoelectrophoresis method for the quantitation of complement C3c in biological fluids.
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- Serum inhibitors of leukocyte chemotaxis in Crohn's disease and ulcerative colitis.
- Defective release of C5a related chemo-attractant activity from complement in Crohn's disease.
- Complement inhibitors and immunoconglutinins in ulcerative colitis and Crohn's disease.
- High Voltage Agarose Gel Electrophoresis in the Study of C 3 Polymorphism
- Humoral immune system activity in inflammatory bowel disease.
- Studies of the C3 polymorphism. Rlationship between C3 phenotypes and rheumatoid arthritis.
- Circulating immune complexes in ulcerative colitis.--II. Correlation with serum protein concentrations and complement conversion products.
- A comparison between clinical state, macroscopic and microscopic appearances of rectal mucosa, and cytologic picture of mucosal exudate in ulcerative colitis.
Cited by
- The immunology of inflammatory bowel disease
- Alterations of the immune system in ulcerative colitis and Crohn's disease.
- High Normal Serum Levels of C3 and C1 Inhibitor, Two Acute-Phase Proteins Belonging to the Complement System, Occur More Frequently in Patients with Crohn's Disease Than Ulcerative Colitis
- Abnormal metabolism of arachidonic acid in chronic inflammatory bowel disease: enhanced release of leucotriene B4 from activated neutrophils.
- Serum interferon activity in inflammatory bowel disease
- Defective modulation of complement in Crohn's disease. C3b opsonization of zymosan by the alternative pathway.
- Assessment of disease severity and activity in inflammatory bowel disease.
- Activation of neutrophil chemotaxis by leukotriene B4 and 5-hydroxyeicosatetraenoic acid in chronic inflammatory bowel disease.
- Inflammatory bowel disease. Part I: Nature and pathogenesis.
- Surface epithelium related activation of complement differs in Crohn's disease and ulcerative colitis.
- The aetiology of Crohn's disease
- Subnormal sensitivity of neutrophils to complement split product C5a in rheumatoid arthritis: relation to complement catabolism and disease extent.
- Activation of classical pathway complement in chronic inflammation. Elevated levels of circulating C3d and C4d split products in rheumatoid arthritis and Crohn's disease.
- Polymorphism of complement C3 in chronic inflammatory bowel disease. Predominance of the C3F gene in Crohn's disease.
- Dissociation between the functional activity and immunoreactive concentration of C1 esterase inhibitor in active and quiescent Crohn's disease.
- Subnormal activation of phagocytes by complement in chronic inflammatory bowel disease? Neutrophil chemotaxis to complement split product C5a.
- Reduced levels of complement C3 after peros administration of ornidazole in normal volunteers
- The Complement System in Inflammatory Bowel Disease
- Crohn's disease: correlation with intestinal symptoms
- Genetics of inflammatory bowel disease
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